No abstract

INTRODUCTION:In this case report, we present a lung transplant recipient in immunosuppressive treatment infected by SARS-CoV-2 who developed abdominal distention of unknown origin. CASE PRESENTATION:In June 2020, a 40-year-old woman underwent a double lung transplant for hereditary pulmonary arterial hypertension (BMPR2 mutation). In November 2020, she was positive for SARS-CoV-2 and developed mild bilateral pneumonia without the necessity of hospitalization. The immunosuppressive maintenance regimen (tacrolimus, prednisolone, and mycophenolate mofetil) was adjusted, and an empiric antibiotic therapy was started. In March 2020, at the follow-up visit, the patient was afebrile but complaining about her abdominal distension. The abdomen was slightly bloated, painful on deep palpation. CT scan of the thorax showed a clear amelioration of the parenchymal findings, whilst the abdominal radiological study detects a widespread submucosal air collection in the transverse and right colon confirmed by a subsequent colonoscopy. Laboratory tests depicted no signs of infection with normal WBC count and serum lactate. For the mild symptoms, the patient was hospitalized with a conservative treatment consisting of bowel rest, parenteral nutrition, adequate hydration, and intravenous antibiotic therapy with ciprofloxacin and metronidazole. In the absence of any signs of complication, the patient was discharged two weeks later with a slight amelioration of the abdominal distension.DISCUSSION: Pneumatosis intestinalis (PI) is a rare condition characterized by the presence of gas within the wall of the large or small bowel. Many aspects of this condition are poorly understood, including etiology, pathogenesis, and clinical implication. It is usually asymptomatic, but a broad clinical spectrum is described in the Literature. Unfortunately, there are no algorithms concerning etiologic diagnosis or treatment. In our patient, PI resulted from lung transplant recipient on immunosuppressive therapy. According to the PI mechanical theory, the persistent cough due to viral pneumonia may have increased intra-abdominal pressure, facilitating the air collection within the bowel wall. Finally, SARS-CoV-2 infection may have been the ultimate trigger. It has been proven that ACE2 is highly expressed in enterocytes and that SARS-CoV-2 uses this as a receptor for its entry process, potentially causing damage to the bowel wall integrity. Additionally, glucocorticoids could prolong SARS-CoV-2 presence in the GI tract, and its potential risk of PI, and viral RNA has been detected for a longer time in the stool of patients on glucocorticoid therapy.CONCLUSIONS: PI is previously described in association with lung transplantation as a rare complication. However, a certain etiology is difficult to highlight although, in our patient, SARS-CoV-2 infection has been an additional risk factor.